Using dissociated fetal mouse spinal cord cells grown in culture, we have investigated aspects of the postsynaptic pharmacology of these mammalian central neurons. In culture these neurons are known to exhibit characteristic responses to the excitatory amino acid glutamate (GLU) and the inhibitory amino acids glycine (GLY), and gamma-aminobutyric acid (GABA). GABAergic inhibition has previously been demonstrated to be decreased by certain convulsant agents (e.g., penicillin and pentylenetetrazol) and increased by some anticonvulsnat agents (diazepam and phenobarbital). We have found that the anticonvulsant agent valproic acid (VPA) specifically augments postsynaptic GABA-mediated inhibition. Such GABA-mediated inhibition may be the common mechanism of action of the major anticonvulsant agents. Delta aminolevulinic acid (ALA), a porphyrin precursor, has been found to attenuate all postsynaptic amino responses but more profoundly affects responses to GABA and GLY, the inhibitory amino acids. ALA was distinctly not GABAergic in action, in contrast to previous reports of such GABAergic responses in invertebrate preparations.